Clearly, established and accepted precepts of present day immunology would not predict either the enhanced growth of B16 tumors in fully chimeric C57/FVB mice or the rejection of these same tumors in the same partially chimeric mice since both of these hosts should be tolerant for the MHC class b haplotype of these tumor cells, as suggested by early transplantation studies with chimeric mice, termed "allophenic" by these authors [9]. The gene discussed is HLA-C; the disease is neoplasm.